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探索慢性肾纤维化与骨形态发生蛋白-7之间的联系。

Exploring the connection between chronic renal fibrosis and bone morphogenic protein-7.

作者信息

Kalluri R, Zeisberg M

机构信息

Harvard Medical School, Program in Matrix Biology, Department of Medicine, Dana 514, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA 02215, USA.

出版信息

Histol Histopathol. 2003 Jan;18(1):217-24. doi: 10.14670/HH-18.217.

Abstract

Tubulointerstitial fibrosis is a hallmark feature of chronic renal injury. Specific therapies to control the progression of renal fibrosis towards end-stage renal failure are still limited. Transforming growth factor-beta1 (TGF-beta1) has been identified as a major mediator of renal fibrosis. Recent reports have suggested that Bone Morphogenic Protein-7 (BMP-7), another member of the TGF-beta superfamily, accelerates repair of acute renal injury and ameliorates progression of chronic renal fibrosis in a variety of animal models. Interestingly, BMP-7, an endogenous molecule which is present in the normal kidney, vastly decreases its expression during renal injury. Although, the mechanism of BMP-7 action in the kidney is not yet fully understood, the idea of an endogenous molecule with reno-protective function is intriguing.

摘要

肾小管间质纤维化是慢性肾损伤的标志性特征。控制肾纤维化向终末期肾衰竭进展的特异性疗法仍然有限。转化生长因子-β1(TGF-β1)已被确定为肾纤维化的主要介质。最近的报道表明,TGF-β超家族的另一个成员骨形态发生蛋白-7(BMP-7)可加速急性肾损伤的修复,并在多种动物模型中改善慢性肾纤维化的进展。有趣的是,BMP-7是一种存在于正常肾脏中的内源性分子,在肾损伤期间其表达会大幅下降。尽管BMP-7在肾脏中的作用机制尚未完全阐明,但具有肾保护功能的内源性分子这一概念很吸引人。

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